Michael (Mike) Bailey, Ph.D., Assistant Professor
Education
Undergraduate:
BS - Winona State University, 1995
Graduate:
MS - Mankato State University, 1997
Ph.D. -
University of Wisconsin-Madison, 2002
Post
Doctoral Training:
The Ohio State University, Dr. John Sheridan
Appointments
Assistant
Professor, Division of Oral Biology
Faculty, Oral
Biology Graduate Program
Member, Institute for Behavioral Medicine Research
Contact Information
Office Address:
257
Institute for Behavioral Medicine Research Building
460
Medical Center Dr.
Columbus OH, 43210
Laboratory Address:
260 &
280 Institute for Behavioral Medicine Research Building
460 Medical Center Dr.
Columbus OH, 43210
Office Phone: (614) 293-4277
Laboratory Phone: (614) 293-4353
Email: Michael.Bailey@osumc.edu
Affiliations &
Memberships
Department of Molecular Virology, Immunology, and Medical
Genetics
Member, Center for Microbial Interface
Biology
Area of Expertise
Animal modeling of stress and
disease
Immunology
Microbiology
Endocrine and Behavioral Assessment of the Stress Response
Teaching
Microbiology and Immunology, Dentistry 646 (Course Director)
Physiology, Dentistry 605 (Lecturer)
Cellular and Molecular Immunology, MVIMG 701 (Lecturer)
Research Interests
Research Summary
Studies in my laboratory are focused on determining the impact
that the intestinal microbiota have on the local mucosal immune
system, and on immune reactivity at systemic sites, particularly
during periods of psychological stress. In past studies, we have
shown that exposure to different types of psychological
stressors changes the community structure of microbiota in the
intestines. Our goal now is to demonstrate that these changes
have significant effects on the health of the host.
Impact of Microbiota on Mucosal Immunity: The
inflammatory bowel diseases involve disrupted homeostatic
interactions between the microbiota and the mucosal immune
system. It is well recognized that symptom severity is worsened
during periods of psychological stress, but whether the stress
response is involved in these disrupted homeostatic interactions
is not known. We have been studying Citrobacter rodentium
infection in mice because the colonic inflammation resembles
components of human inflammatory bowel disease. In our studies,
exposing mice to an experimental stressor during oral challenge
with C. rodentium significantly increases the pathogen-induced
colitis. Our preliminary studies indicate that the
stressor-induced increase in colitis is dependent upon
stressor-induced alterations of the microbiota, thus
demonstrating a link between stress, alterations in the
microbiota, and exacerbation of colonic inflammation. Current
studies are focused on further characterizing the colonic
inflammation, including determining the impact of the stress
response on colonic epithelial cells and lamina propria
leukocytes. Studies are also focused on determining which
members of the microbiota contribute to the enhanced colonic
inflammation.
Impact of Microbiota on Systemic Immunity: The
stress response is often thought of as suppressing immune
activity. However, there is accumulating evidence that in
addition to suppressing immune function, the stress response can
also enhance immune activity. And, although many of the
mechanisms by which the stress response suppresses immunity are
known, such as by the action of stress-responsive glucocorticoid
hormones, the mechanisms by which the stress response enhances
immune activity are not well understood. We have been using a
murine social stressor, called social disruption, to study how
stressor exposure enhances the ability of splenic macrophages to
kill a target microbe, namely Escherichia coli. Our data
indicate that stressor exposure increases the splenic macrophage
oxidative burst, resulting in increased production of
superoxide, and increases iNOS gene expression, resulting in
increased production of nitric oxide. This increased activity
ultimately results in the production of the highly microbicidal
compound, peroxynitrite. Our current studies are focused on
determining how the stress response enhances macrophage
peroxynitrite production, and indicate that the intestinal
microbiota are involved. Our goal is to determine how the
microbiota can enhance splenic macrophage activity during
stressor exposure.
Publications
M.T.
Bailey, S. E. Dowd, J.D. Galley, A.R. Hufnagle, R.G. Allen,
and M. Lyte (2011). Exposure to a social stressor alters the
structure of the intestinal microbiota: Implications for
stressor-induced immunomodulation. Brain, Behavior, and
Immunity. 25(3): 397-407. (Journal Impact Factor:
5.06).
*This manuscript received a special commentary published in
the journal BBI.
M.T. Bailey, S.E. Dowd, N.M.A. Parry, J.D. Galley, D.B.
Schauer, and M. Lyte. (2010). Stressor exposure disrupts
commensal microbial populations in the intestines and leads to
increased colonization by Citrobacter rodentium. Infection
and Immunity. 78(4): 1509-1519.
(Chosen as a Spotlight Contribution) (Journal Impact
Factor: 4.2).
M. T. Bailey, Engler, H., Powell, N.D., Padgett, D.A.,
and J. F. Sheridan. (2007). Repeated social defeat increases the
bactericidal activity of splenic macrophages through a toll-like
receptor dependent pathway. American Journal of Physiology;
Regulatory, Integrative, and Comparative Physiology;
293(3):R1180-90. (Journal Impact Factor: 3.06).
M.T. Bailey, J.E. Walton, Z. Weil, and R.J. Nelson.
(2010). Photoperiod modulates gut bacteria composition in male
Siberian hamsters (Phodopus sungorus). Brain, Behavior and
Immunity. 24(4): 577-584. (Journal Impact Factor:
5.06).
M.T.
Bailey, Kierstein, S., Spaits, M., Kinsey, S.G., Sheridan,
J.F., Panettieri, R.A., and Haczku, A. (2009). Social stress
enhances allergen-induced airway inflammation in mice.
Journal of Immunology. 182(12): 7888–7896. (Journal
Impact Factor: 5.65).
